Visual System Disease

Glyoxal (40% w/w in water) is an α-oxoaldehyde that inhibits Aldose Reductase, Glutathione Reductase, and NADPH synthase. Glyoxal (40% w/w in water) exhibits cytotoxicity, triggers oxidative stress, induces ROS accumulation, lipid peroxidation, mitochondrial membrane potential collapse, DNA damage, apoptosis, and massive production of advanced glycation end products (AGEs). Glyoxal (40% w/w in water) depletes glutathione and activates MAPK phosphorylation. It has lower toxicity as a fixative than paraformaldehyde (PFA) and serves as a precursor for the synthesis of oxalates and dietary carcinogens. Glyoxal (40% w/w in water) is suitable for research related to calcium oxalate kidney stones, diabetes, atherosclerosis, cardiovascular diseases, retinopathy, and cataracts.

Fluoflavine (ML-090) is a selective NOX1 inhibitor and reactive oxygen species inhibitor. Fluoflavine reduces reactive oxygen species production, NOX1-mediated downstream signaling events, and oxygen-glucose deprivation-induced retinal ganglion cell death. Fluoflavine inhibits NADPH oxidase activity and pathological retinal neovascularization induced by oxygen-induced retinopathy in the retinas of ischemic mice. Fluoflavine can be used in studies related to retinal ischemia-reperfusion injury and proliferative retinopathy.

Avacincaptad pegol (Izervay) is a selective inhibitor targeting complement component C5, and is a pegylated ribonucleic acid aptamer. Avacincaptad pegol inhibits the cleavage of C5 into pro-inflammatory C5a and C5b, which forms the membrane attack complex (C5b-9), thereby reducing inflammatory cell recruitment and retinal cell damage. Avacincaptad pegol can slow the growth of geographic atrophy (GA) lesions and reduce the risk of persistent vision loss. Avacincaptad pegol can be used in research of geographic atrophy associated with age-related macular degeneration (AMD) and has been approved by the FDA.

Udonitrectag (REC 0559) is a nerve growth factor peptide mimetic and a TrkA receptor binder. Udonitrectag binds to the TrkA receptor, thereby mimicking anti-Apoptotic activity and corneal trophic activity. Udonitrectag promotes the healing of corneal epithelium and stroma. Udonitrectag is applicable to research related to neurotrophic keratitis.

AZ14145845 is an orally active dual-target type 1½ kinase inhibitor of Mer/Axl, which inhibits Mer kinase (pIC₅₀ = 9.0) and Axl kinase (pIC₅₀ = 7.9) with high selectivity over Flt3 and Tyro3. AZ14145845 suppresses Mer- and Axl-dependent proliferation in Ba/F3 cells and inhibits efferocytosis in macrophages. AZ14145845 reduces the phagocytosis of photoreceptor outer segments by polarized human retinal epithelial cells. AZ14145845 inhibits tumor growth and induces tumor regression in vivo, and its combination with anti-PD1 antibody and ionizing radiation improves the survival rate of mice with colorectal cancer. AZ14145845 causes retinal degeneration in mice, with pathological changes similar to those in MERTK loss-of-function models. AZ14145845 can be used in studies related to retinal degeneration, lymphoma and colorectal cancer.

Wolfberry Extract is the extract of Wolfberry. Wolfberry Extract exhibits antioxidant and anti-inflammatory effects. Wolfberry Extract can be used as a dietary supplement for the research of age-related macular degeneration and inflammatory diseases.

Glutathione trisulfide (GSSSG) is an orally active, blood-brain barrier permeable neuroprotective agent. Glutathione trisulfide inactivates intracellular tyrosinase, regulates the expression of Cars2, Cbs, MITF and TYR, inhibits α-MSH (HY-P0252)-induced melanogenesis, and restores intracellular persulfide levels reduced by α-MSH. Glutathione trisulfide scavenges free radicals, quenches ROS, reduces Paclitaxel (HY-B0015)-induced superoxide production, upregulates the expression of antioxidant protein genes, and inhibits oxidative stress-induced cell death. Glutathione trisulfide promotes ERK1/2 activation, prevents NF-κB p65 activation, inhibits TAK1 phosphorylation, reduces pro-inflammatory cytokine expression, and blocks microglial activation. Glutathione trisulfide can be used in research related to dry age-related macular degeneration, inflammation-associated eye diseases, Alzheimer's disease, Parkinson's disease, etc.

Libvatrep (SAF312) is a non-competitive TRPV1 antagonist with an IC₅₀ of 0.35-0.69 µM in HEK293T cells. It binds to the vanilloid pocket and an allosteric site, preventing S4/S5 conformational changes and channel opening. Libvatrep can be used for research on ocular surface pain and eye pain after photorefractive keratectomy.

Bevasiranib sodium is a siRNA that targets and silences VEGF-A. Bevasiranib sodium activates the RNA-induced silencing complex to degrade VEGF-A mRNA, mediates TLR3-related inhibition of choroidal neovascularization, and triggers RNA interference-mediated gene silencing through endogenous eukaryotic RNAi mechanisms. After intravitreal injection, Bevasiranib sodium distributes to various ocular tissues and resists degradation by intraocular nucleases, reducing choroidal neovascularization area and alleviating vascular leakage. Bevasiranib sodium can be used in research related to macular degeneration.

Epsilon-(gamma-glutamyl)-lysine TFA (H-Glu (H-Lys-OH)-OH) is an isodipeptide formed during the proteolytic degradation of proteins containing Nε-(γ-glutamyl)-lysine cross-links. Epsilon-(gamma-glutamyl)-lysine TFA serves as a substrate for γ-glutamylamine cyclotransferase, which specifically cleaves it. Epsilon-(gamma-glutamyl)-lysine TFA is applicable to studies related to transglutaminase-mediated protein cross-linking and turnover, γ-glutamylamine cyclotransferase activity, glaucoma, and tissue scar formation.

SNJ-1945 is an orally active, blood-brain barrier-penetrant Calpain inhibitor. SNJ-1945 inhibits Cathepsin L, Cathepsin B, and Ca²⁺ -independent proteases. SNJ-1945 suppresses ROS production and downregulates Cyclooxygenase-2 and Caspase-1. SNJ-1945 alleviates left ventricular systolic dysfunction, reduces cerebral ischemia-induced injury, and decreases the score of experimental autoimmune encephalomyelitis in mouse models. SNJ-1945 can be used in research related to post-cardiac arrest reperfusion injury, Parkinson's disease, multiple sclerosis, and proliferative retinopathy.

PG-901 is a full, selective MC5R agonist (EC₅₀ = 0.072 nM for hMC5R). PG-901 is also a full antagonist at the hMC3R and the hMC4R (K_b: 1.0 nM and 0.53 nM, respectively). PG-901 significantly diminishes Cytokines (IL-1α, IL-1β, IL-6). PG-901 increases glucose tolerance, reduces blood glucose, decreases retinal damage.

Hyaluronic acid, low endotoxin (Hyaluronan, low endotoxin) is a biopolymer composed of repeating disaccharide units containing low levels of endotoxin. Hyaluronic acid is a major component of the extracellular matrix (ECM). It is synthesized on the plasma membrane. Hyaluronic acid exerts its effects by binding to receptors CD44 and RHAMM. Hyaluronic acid activates PI3K-Akt signaling. Hyaluronic acid also enhances cell invasion and angiogenesis by promoting or stimulating the binding of proteolytic MMP-9 to the cell surface. Elevated hyaluronic acid levels are associated with tumor cell growth, adhesion, migration, invasion, and angiogenesis in digestive system cancers. Hyaluronic acid is involved in tissue remodeling and rapid cell proliferation in several physiological processes, including embryonic morphogenesis and wound healing. Hyaluronic acid can be used as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid can be used as a drug delivery carrier for sodium butyrate, enhancing its anti-proliferative activity against breast cancer cell lines. Hyaluronic acid can lubricate the corneal endothelium. Hyaluronic acid can improve tissue hydration and enhance the resistance of cells to mechanical damage. Hyaluronic acid has been conjugated with antibodies to ensure that the active compound continues to exert its effects at the site of inflammation. Hyaluronic acid can be used in research in the fields of osteoarthritis, ophthalmology, cosmetic dermatology, oncology, and liver diseases.

Nimucitinib is a selective JAK inhibitor with potent tear secretion-promoting activity. Nimucitinib downregulates relevant signal transduction pathways by inhibiting the catalytic activity of JAK family tyrosine kinases. Nimucitinib promotes tear secretion in rabbits and inhibits corneal injury in rats. Nimucitinib can be used in dry eye-related research.

S-Ac7-DOG is a cationic lipid with biodegradability, low immunogenicity and high nucleic acid transfection capacity, which is commonly used to construct lipid nanoparticles for nucleic acid molecule delivery. S-Ac7-DOG can bind to mRNA, microRNA and self-amplifying RNA through electrostatic interaction. Lipid nanoparticles formed by S-Ac7-DOG enter cells via an energy-dependent endocytic pathway, release nucleic acid cargos, induce antigen-specific CD8⁺ T cell responses, promote the generation of precursor memory T cells, and regulate neuroinflammatory pathways. S-Ac7-DOG can be used in the research of retinal diseases, neuroinflammation and cancer.

Ultevursen (QR-421a) is a splice-modulating antisense oligonucleotide targeting exon 13 of the USH2A gene, which restores the functional expression of Usherin protein by inducing exon skipping. Ultevursen binds to USH2A pre-mRNA and modulates the splicing process to specifically skip exon 13 carrying the pathogenic mutation c.2299delG, generating an in-frame transcript and a truncated yet functionally normal protein. Ultevursen exhibits concentration-dependent exon skipping activity in human cells and retinal organoid models, and restores Usherin expression and retinal function in zebrafish and gene-edited mouse models. Ultevursen can be used for related research on type 2 Usher syndrome and non-syndromic retinitis pigmentosa.

Ultevursen sodium (QR-421a) is a splice-modulating antisense oligonucleotide targeting exon 13 of the USH2A gene, which restores the functional expression of Usherin protein by inducing exon skipping. Ultevursen sodium binds to USH2A pre-mRNA and modulates the splicing process to specifically skip exon 13 carrying the pathogenic mutation c.2299delG, generating an in-frame transcript and a truncated yet functionally normal protein. Ultevursen sodium exhibits concentration-dependent exon skipping activity in human cells and retinal organoid models, and restores Usherin expression and retinal function in zebrafish and gene-edited mouse models. Ultevursen sodium can be used for related research on type 2 Usher syndrome and non-syndromic retinitis pigmentosa.

ZAPA sulfate is a competitive GABA_C receptor antagonist.

L-Tryptophanamide is an amide derivative of tryptophan. L-Tryptophanamide has potential effects in inducing cell proliferation, apoptosis, necrosis, and angiogenesis-related activities. L-Tryptophanamide also exhibits anti-Leishmania activity. L-Tryptophanamide can be used in research on ulcerative colitis, wet age-related macular degeneration, skin diseases, chronic obstructive pulmonary disease, and leishmaniasis.

Sphingomab (LT1002) is a mouse-derived IgG1 κ monoclonal antibody and also an inhibitor targeting S1P, with high affinity for S1P and a K_d value of 0.03 ± 0.002 nM. Sphingomab blocks S1P-mediated IL-8 release in ovarian cancer cells. Sphingomab exhibits anti-angiogenic activity in a mouse model of choroidal neovascularization. Sphingomab reduces peripheral blood lymphocyte counts. Sphingomab can be used in the research of ovarian cancer and age-related macular degeneration.